2014 Fiscal Year Final Research Report
Analysis of replication stress responses caused by oncogenic signals
| Project/Area Number |
24700952
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Carcinogenesis
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| Research Institution | Gunma University |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Keywords | 複製ストレス / Y-familyポリメラーゼ / 発がん遺伝子 |
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| Outline of Final Research Achievements |
DNA rereplication is a major type of oncogene-induced aberrant replication and plays an important role in genomic instability during tumor development. Rereplication causes DNA double strand breaks, resulting in copy number changes and genomic rearrangements. However, little is known on what DNA polymerases are involved in rereplication. Normal DNA replication is catalyzed by high-fidelity replicative polymerases, Pol ε and Pol δ. Y-family polymerases (Y-Pols) are the major group of low-fidelity polymerases whose main function is bypass of replication blocks at sites of DNA damages, i.e. translesion synthesis. We found that Y-Pols as well as replicative polymerases, participate in rereplication.
The present findings have important mechanistic implications in genomic instability during tumorigenesis. Speculatively, the involvement of Y-Pols in rereplication may account for frequent occurrence of single nucleotide variations in conjunction with gene rearrangements in cancer genomes.
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| Free Research Field |
分子細胞生物学
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